ABRO1 suppresses tumourigenesis and regulates the DNA damage response by stabilizing p53

Jianhong Zhang, Mengmeng Cao, Jiahong Dong, Changyan Li, Wangxiang Xu, Yiqun Zhan, Xiaohui Wang, Miao Yu, Changhui Ge, Zhiqiang Ge and Xiaoming Yang ()
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Jianhong Zhang: State Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing Institute of Radiation Medicine
Mengmeng Cao: School of Chemical Engineering and Technology, TianJin University
Jiahong Dong: The General Hospital of Chinese People’s Liberation Army
Changyan Li: State Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing Institute of Radiation Medicine
Wangxiang Xu: State Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing Institute of Radiation Medicine
Yiqun Zhan: State Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing Institute of Radiation Medicine
Xiaohui Wang: State Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing Institute of Radiation Medicine
Miao Yu: State Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing Institute of Radiation Medicine
Changhui Ge: State Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing Institute of Radiation Medicine
Zhiqiang Ge: School of Chemical Engineering and Technology, TianJin University
Xiaoming Yang: State Key Laboratory of Proteomics, Beijing Proteomics Research Center, Beijing Institute of Radiation Medicine

Nature Communications, 2014, vol. 5, issue 1, 1-15

Abstract: Abstract Abraxas brother 1 (ABRO1) has been reported to be a component of the BRISC complex, a multiprotein complex that specifically cleaves ‘Lys-63’-linked ubiquitin. However, current knowledge of the functions of ABRO1 is limited. Here we report that ABRO1 is frequently downregulated in human liver, kidney, breast and thyroid gland tumour tissues. Depletion of ABRO1 in cancer cells reduces p53 levels and enhances clone formation and cellular transformation. Conversely, overexpression of ABRO1 suppresses cell proliferation and tumour formation in a p53-dependent manner. We further show that ABRO1 stabilizes p53 by facilitating the interaction of p53 with USP7. DNA-damage induced accumulation of endogenous ABRO1 as well as translocation of ABRO1 to the nucleus, and the induction of p53 by DNA damage is almost completely attenuated by ABRO1 depletion. Our study shows that ABRO1 is a novel p53 regulator that plays an important role in tumour suppression and the DNA damage response.

Date: 2014
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DOI: 10.1038/ncomms6059

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